ST elevation myocardial infarction complications
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| Myocardial infarction Classification and external resources | |
| ICD-10 | I21.-I22. |
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| ICD-9 | 410 |
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Introduction
Complications may occur immediately following the heart attack (in the acute phase), or may need time to develop (a chronic problem). After an acute myocardial infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery or in the same zone if there are any live cells left in the infarct. Circulatory failure from either severe left ventricular (LV) dysfunction or one of the mechanical complications of acute myocardial infarction is responsible for majority of fatal events.[1]
In general, there are 5 different groups of complications in the setting of an acute myocardial infarction.
A.Ischemic
B.Mechanical
C.Arrhythmic
D.Embolic
E.Inflammatory disturbances (e.g. pericarditis)
A. Ischemic Complications
Extension of Infarct Area
Infarct area extension is a progressive increase in myocardial necrosis within the infarct zone of the current myocardial infarction. This may present as an additional myocardial infarction, that extends and involves the adjacent myocardium or as a subendocardial myocardial infarction that becomes transmural.
Re-occlusion of infarct related arteries (IRAs) occurs in 5-30% of patients after fibrinolytic therapy. These patients tend to have a poorer outcome.[1] Reinfarction is more common in patients with diabetes mellitus or prior myocardial infarction.[1]
Recurrent Myocardial Infarction (Re MI)
Myocardial infarction in a separate territory (recurrent myocardial infarction) may be difficult to diagnose in the first 24-48 hours after the initial event. Multi vessel coronary artery disease is common in patients presenting with acute myocardial infarction. In fact, angiographic evidence of complex or ulcerated plaques in non IRAs is present in up to 40% of patients with acute myocardial infarction.
Postinfarction Angina
Angina that occurs within a few hours to 30 days after acute myocardial infarction is defined as postinfarction angina. The incidence of post infarction angina is greatest in patients with non ST segment elevation MI (NSTEMI) (approximately in 25% of cases) and in those treated with fibrinolytics, compared with mechanical revascularization.
Pathophysiology
Reinfarction occurs more frequently when an infarct related artery (IRA) reoccludes than when it remains patent; however, re-occlusion of an IRA does not always cause reinfarction because of collateral circulation. After fibrinolytic therapy, reocclusion is found on 5% to 30% of angiograms and is associated with worse outcome.
The pathophysiologic mechanism of post infarction angina is similar to that of unstable angina and should be similarly managed. Patients with post infarction angina have a worse prognosis (sudden cardiac death, reinfarction, and acute cardiac events).
Signs and Symptoms
Patients with infarct extension or post infarction angina usually have continuous or recurrent chest pain, with elevation in creatine kinase (CK). Static ECG occasionally shows new changes. Continuous ST Segment Monitoring may provide early and reliable information.
Diagnostic Testing
The diagnosis of infarct expansion, re-infarction, or post-infarction ischemia can be made with echocardiography or nuclear cardiac imaging.
A new wall motion abnormality, larger infarct size, new area of infarction, or persistent reversible ischemic changes help to substantiate the diagnosis.
The myocardial component (Creatine Kinase Myocardial Band = CK-MB) of Creatine Kinase (CK), is a more useful marker for tracking ongoing infarction than troponins (cTnI, cTnT) for their shorter half life.
Changes (sharp rising and falling) in CK-MB levels suggest infarct expansion or recurrent infarction. Frequently ≥50% elevations of previous CK-MB values are diagnostic for reinfarction.
Treatment and Management
Medical therapy with aspirin, heparin, nitrates, and beta blockers is indicated for patients who had an acute myocardial infarction and have ongoing ischemic symptoms.
An intra aortic balloon pump (IABP) should be inserted (in cathlab) in patients with unstable hemodynamic conditions or severe left ventricular systolic dysfunction (e.g. low LV EF).
Performing a coronary angiography is required to diagnose underlying pathology (to avoid contrast related overload and preventing kidney functions, this should be done after stabilization with medical therapy in patients with severe pulmonary edema). Emergency coronary angiography should be performed in unstable patients. Surgical and/or percutaneous coronary revascularization is associated with improved prognosis.
B. Mechanical Complications of Acute Myocardial Infarction
Mechanical complications of acute myocardial infarction include rupture of ventricular septum or papillary muscle (papillary muscle rupture or papillary muscle dysfunction more frequently occur and may cause acute mitral regurgitation), free wall rupture, pseudoaneurysm formation, left ventricular (LV) failure, cardiogenic shock, right ventricular (RV) failure, ventricular aneurysm, and dynamic left ventricular outflow tract (LVOT) obstruction. [1]
Rupture of Ventricular Septum
Prevalence
Rupture of ventricular septum occurred among 1% to 2% of patients after acute MI in the prethrombolytic era. [1] The incidence has dramatically decreased with reperfusion therapy. The GUSTO 1 trial demonstrated a Rupture of ventricular septum incidence of approximately 0.2%. [1] [1]
Rupture of ventricular septum more frequently occur in older age, female, hypertensive, non smoker individuals, and who have anterior infarction, increased heart rate, and worse Killip class at admission.
Rupture of ventricular septum may develop as early as 24 hours after MI; it was commonly seen 3 to 7 days after MI in the prefibrinolytic era and currently is seen 2 to 5 days after MI.2 Fibrinolytic therapy is not associated with increased risk of rupture of ventricular septum.[1]
Pathophysiology
Rupture of interventricular septum frequently seen in anterolateral myocardial infarction; almost always occurs in the setting of a transmural MI and usually occurs at the border of normal and infarcted myocardium around the apical septum in patients with anterior MI, and it affects the basal posterior septum in patients with inferior MI.
Sometimes, the interventricular septal rupture is not a single defect; approximately 30-40% of cases have a meshwork of channels.
Signs and Symptoms
In early phase of interventricular septal rupture process, patients may not show any significant symptoms, and appear relatively comfortable but rapid recurrence of angina, hypotension, cardiogenic shock, or pulmonary edema may develop later in the course.
Diagnosis of interventricular septal rupture
Rupture of the ventricular septum is often accompanied by a new harsh holosystolic murmur that best heard at the left lower sternal border. The murmur is accompanied by a thrill in 50% of cases. Usually, this sign accompanied by a rapid worsening hemodynamic profile and biventricular failure. Therefore, it is important that all patients with myocardial infarction have a well documented complete cardiac examination at presentation (baseline).
Approximately 40% of patients may have atrioventricular A-V nodal or infranodal conduction abnormalities. Monitoring of static ECGs may help to show and help to follow these changes.
Echocardiography with color Doppler flow imaging is the test of choice for diagnosis of ventricular septal rupture. Two-dimensional and Doppler echocardiographic examinations help to define left and right function (these are important determinants of mortality) as well as the size of the defect and degree of left to right shunt with a flow assessment through the pulmonary and aortic valves.
In presence of any difficulties transesophageal echocardiography (TEE) is helpful to assess the ventricular septal defect.
Magnetic resonance imaging is particularly useful in the detection and assessment of interventricular septal rupture. The role of MRI in this situation is valuable the most when echocardiography fails to demonstrate defects which are located immediately below the pulmonary valves.
Ventricular Septal Defect can also be diagnosed by demonstrating a step up in oxygen saturation in the right ventricle and pulmonary artery (PA) on right heart catheterization. The location of the step-up is important, as there have been rare case reports of peripheral PA step-ups due to acute mitral regurgitation (MR). Diagnosis involves fluoroscopically guided measurement of oxygen saturation in the superior and inferior vena cava, right atrium, right ventricle, and pulmonary artery.
More than 8% difference in oxygen saturation of occurs between the right atrium and the pulmonary artery in presence of a left-to-right shunt across the ventricular septum. A shunt fraction can be calculated as follows:
Pulmonary Flow / Systemic Flow = Arterial O2 Saturation (SaO2) – Mixed Venous Oxygen Saturation / Pulmonary Venous Oxygen Saturation - Pulmonary Arterial Oxygen Saturation
Results ≥2 show a considerable shunt which may poorly tolerated by patient.
Ventricular septal rupture1.jpg
Pathological Findings
Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission. © PEIR, University of Alabama at Birmingham, Department of Pathology
 Heart, Acute MI, Ventricular septum rupture at posterior wall. |
 Gross; acute myocardial infarction with ventricular septal rupture |
 Acute MI, rupture of the ventricular septum. A close up view. |
Treatment and Management
If patient’s hemodynamic conditions permit, early surgical closure is the best treatment of choice. Although, initial reports suggests delaying surgery resulted in lower surgical mortality rates [1] these benefits are likely the result of selection biases, because the mortality rate among patients with interventricular septal rupture in the setting of acute myocardial infarction who treated medically is 24% at first 72 hours, and 75% at within 3 weeks. [1] Therefore, patients with interventricular septal rupture in the setting of acute myocardial infarction should be considered for urgent surgical repair. Regardless of the infarct localization and hemodynamic condition of the patient, surgery should always be considered as it is associated with a lower mortality rate than conservative management. [1]
Cardiogenic shock and multisystem failure from interventricular septal rupture are associated with high mortality rates. This further supports early surgical intervention before complications develop. [1]
Mortality is the highest in patients with basal septal rupture associated with inferior myocardial infarctions (70% vs. 30% when compared in patients with anterior myocardial infarctions).
In presence of mitral regurgitation the mortality rate is particularly higher due to increased technical difficulty and need for mitral valve repair or replacement. [1]
The patient should always been supported with Intensive medical management before the surgical therapy. In the absence of significant aortic regurgitation, the intra aortic balloon pump (IABP) should be inserted as a bridge to the surgical procedure.
The insertion of IABP will decrease systemic vascular resistance and shunt fraction while increasing coronary perfusion and maintaining adequate blood pressure. After insertion of an IABP, vasodilators can be used with close hemodynamic monitoring.
Vasodilator drugs also reduce left-to-right shunt and increase systemic vascular flow by reducing the systemic vascular resistance. The vasodilator drug of choice is intravenous (IV) form of sodium nitroprusside. The starting dose is 0.5-1.0 µg/kg/min and should be titrated to maintain mean arterial pressure (MAP) at 60-75 mm Hg.
Acute Mitral Regurgitation
Incidence
The occurrence of mild to moderate severity of mitral regurgitation is 13-45% in patients with acute myocardial infarction. Mitral regurgitation occurs after an acute myocardial infarction, it predicts poorer prognosis. [1] [1] Although most mitral regurgitations are transient and asymptomatic, mitral regurgitation caused by frank papillary muscle rupture is a life-threatening complication. [1]
Although, administration of fibrinolytic agents decrease the incidence of rupture; however, rupture may occur earlier in the setting of myocardial infarction.
In the pre-fibrinolytic era, the frequent occurrence of papillary muscle rupture had been reported between day 2 and 7; however, results of the SHOCK Trial demonstrated a median time to papillary muscle rupture of 13 hours. [1] Incidence of papillary muscle rupture is approximately 7% in patients with cardiogenic shock and contributes 5% of the mortality after acute myocardial infarction. [1] [1]
Pathophysiology of mitral regurgitation
Mitral regurgitation can occur as a result of multiple mechanisms including:
Burch et al first proposed that papillary muscle dysfunction could be due to either mitral valve prolapse or incomplete mitral valve closure[1] [1]
- Left ventricular dilatation
- Papillary muscle ischemia
- mitral annular dilatation secondary to left ventricular dilatation.
- Non ischemic papillary muscle atrophy.
- Congenital abnormalities of papillary muscles or tendons.
- Endocardial diseases (endocarditis, fibroelastosis).
- Expansion or hypertrophic cardiomyopathy.
- Papillary muscle contraction coordination abnormalities
- Partial or complete rupture of Papillary muscle or tendons as a result of papillary muscle infarction.
The anterolateral papillary muscle has a dual blood supply, being perfused by the left anterior descending and left circumflex coronary arteries. Papillary muscle rupture occur the most in patients with inferior myocardial infarction. Because of its single blood supply through the posterior descending coronary artery, the posteromedial papillary muscle is most frequently involved. [1]
Clinical Presentation
Complete rupture of all papillary muscles is rare and usually results in immediate pulmonary edema, cardiogenic shock, and death.
Physical examination demonstrates a new [[pansystolic murmur], which is audible at the cardiac apex and radiates to the axilla or at the base of the heart. If a posterior papillary muscle rupture is present, the murmur radiates to the left sternal border and may be confused with the murmur of ventricular septal rupture or aortic stenosis.
The intensity of the murmur does not always show the severity of mitral regurgitation. In patients with severe heart failure, low cardiac output, or elevated left atrial pressures, the murmur may be soft or absent.
Diagnostic Testing
The ECG usually shows evidence of recent inferior or posterior MI.
The chest radiograph reveals pulmonary edema. Focal pulmonary edema may occur in the right upper lobe when flow is directed at the right pulmonary veins.
The diagnostic test of choice is two-dimensional echocardiography with Doppler and color-flow imaging.
In severe mitral regurgitation, the mitral valve leaflet is usually flail. Color-flow imaging is useful in distinguishing papillary muscle rupture with severe mitral regurgitation from VSD.
If transthoracic echocardiography cannot fully appreciate the amount of mitral regurgitation in patients with posteriorly directed jet flow the transesophageal echocardiography is useful to clarify all related anatomic conditions.
Additionally, hemodynamic monitoring with a pulmonary artery catheter (Swan-Ganz catheter or a multipurpose one) may reveal large V waves (>50 mm Hg) in the pulmonary capillary wedge pressure (PCWP).
Treatment and Management
Patients with papillary muscle rupture should be rapidly identified and should receive aggressive medical treatment while being considered for surgery. Medical therapy includes vasodilator therapy. Sodium nitroprusside is useful in the treatment of acute mitral regurgitation because it decreases systemic vascular resistance, thereby reducing the regurgitant fraction and increasing the forward stroke volume and cardiac output. Sodium nitroprusside can be started at 0.5-1.0µg/kg/min and titrated to maintain a mean arterial pressure of 60-75 mm Hg.
An IABP should be inserted to decrease LV afterload, improve coronary perfusion, and increase forward cardiac output. Patients with hypotension may better tolerate vasodilators after insertion of an IABP.
Patients with papillary muscle rupture should be considered for emergency surgery because the prognosis is poor among medically treated patients. Performing coronary angiography is necessary before surgical repair, as revascularization during mitral valve replacement (MVR) is associated with improved short and long term mortality.[1]
Myocardial Rupture
This may occur in the free walls of the ventricles, the septum between them, the papillary muscles, or less commonly the atria. Rupture occurs because of increased pressure against the weakened walls of the heart chambers due to heart muscle that cannot pump blood out effectively. The weakness may also lead to ventricular aneurysm, a localized dilation or ballooning of the heart chamber.
Incidence of Myocardial Rupture
Myocardial rupture is most common three to five days after myocardial infarction, commonly of small degree, but may occur one day to three weeks later (cardiac rupture may occur within 5 days of MI in 50% of patients and within 2-3 weeks in 90% of them). In the modern era of early revascularization and intensive adjunctive pharmacotherapy as treatment for acute myocardial infarction, the incidence of myocardial rupture is about 1% of all myocardial infarctions and accounts for approximately 10% of mortality. Free wall rupture occurs only among patients with transmural myocardial infarction. [1]
Risk factors include advanced age, female gender, hypertension, first MI, and poor coronary collateral vessels.
Pathophysiology cardiac rupture
Although myocardial rupture accounts for part of the early (first 24 hours) mortality risk among patients treated with fibrinolytic agents, the overall incidence of free wall rupture is not greater in patients treated with fibrinolytic drugs.[1] Any wall can be involved, but cardiac rupture most commonly occurs in the lateral wall.
Myocardial rupture occurs at three distinct intervals with three distinct pathologic subsets:
- Type I rupture; increases with the use of fibrinolytic drugs. It occurs early (within the first 24 hours) and is a full-thickness rupture.
- Type II rupture; occurs within 1 to 3 days post myocardial infarction and is a result of erosion of the myocardium at the infarction site.
- Type III rupture; occurs late (days 5-10) and is located at the border zone of the infarction and normal myocardium. The reduction in Type III ruptures due to fibrinolytic therapy results in no change in the overall free wall rupture rate. It has been postulated that Type III ruptures can occur as a result of dynamic LVOT obstruction, which leads to increased wall stress. [1]
Signs and Symptoms
Sudden onset of chest pain with straining or coughing may herald the onset of myocardial rupture. Patients with acute myocardial rupture often develop electromechanic dissociation, cardiogenic shock, and sudden cardiac death. Other patients may have a more subacute course as a result of a contained rupture (pseudoaneurysm). They may complain of pain consistent with pericarditis, nausea, and develop hypotension. In a study evaluating 1,457 patients with acute myocardial infarction, 6.2% of patients had free wall rupture. Approximately one third of these patients presented with a subacute course. [1]
Jugular venous distention, pulsus paradoxus, diminished heart sounds, and a pericardial rub suggest subacute rupture. New to-and-fro murmurs may be heard in patients with subacute rupture or pseudoaneurysm. A junctional or idioventricular rhythm, low-voltage complexes, and tall precordial T waves may be evident on ECG. Additionally, a large number of patients develop transient bradycardia just before rupture. [1]
Diagnostic Testing
Although there is often insufficient time for diagnostic testing in the management of patients with acute rupture, a bedside echocardiography is the test of choice. Echocardiography may demonstrate a pericardial effusion with findings of cardiac tamponade. These findings include right atrium and right ventricular diastolic collapse, dilated inferior vena cava, and marked respiratory variation in mitral and tricuspid inflow. Additionally, a pulmonary artery (PA) catheter may reveal hemodynamic signs of cardiac tamponade, with equalization of the right atrium, right ventricular diastolic pressure, and pulmonary capillary wedge pressure (PCWP).
Management and Treatment
The goal of therapy is to diagnose the problem quickly and perform early emergency cardiac surgery to correct the rupture. Emergency pericardiocentesis may be performed on patients with cardiac tamponade and severe hemodynamic compromise while arrangements are being made for transport to the operating room.
Pericardiocentesis may be dangerous due to reopening of the communication with the pericardium as the intrapericardial pressure is relieved.
Medical management has no role in the treatment of these patients except for vasopressors to maintain blood pressure as the patient is transported to the operating room.
Pathological Findings
Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission. © PEIR, University of Alabama at Birmingham, Department of Pathology
 Gross horizontal section of ruptured anterolateral infarct |
 Gross, Acute MI, external view of ruptured myocardial infarction near apex |
 Gross natural color external view of heart with repair patch over ruptured anterior infarction. A horizontal section of fixed ventricles |
 IAcute MI:Gross fixed tissue horizontal section ventricles. A large anterior infarct rupture with repair patch. |
 Gross natural color close-up of apical patch repair of ruptured infarct seen from right ventricle side septal rupture |
Pseudoaneurysm
Pathophysiology
Pseudoaneurysm is caused by a contained rupture (preserved) of the left ventricular free wall. The aneurysm may remain small or undergo progressive enlargement. The outer walls are formed by the pericardium and mural thrombus. The pseudoaneurysm communicates with the body of the left ventricle through a narrow neck, the diameter of which is less than 50% of the diameter of the fundus.
Signs and Symptoms
Pseudoaneurysms may remain clinically silent and be discovered during routine investigations; however, some patients may have recurrent tachyarrhythmia and heart failure. Some patients may have systolic, diastolic, and/or ejection, regurgitation murmurs related to blood flow across the narrow neck of the pseudoaneurysm during systole and diastole.
A chest radiograph may show cardiomegaly with an abnormal bulge on the cardiac border. There may by persistent ST segment elevation on ECG. The diagnosis can be confirmed by echocardiography, magnetic resonance imaging, or computed tomography.
Management and Treatment
Spontaneous rupture may occur without warning in approximately one third of patients with a pseudoaneurysm. Therefore, surgical intervention is recommended to prevent sudden death for all patients, regardless of symptoms or the size of the aneurysm.
Left Ventricular Failure and Cardiogenic Shock
Incidence of Left Ventricular Failure and Cardiogenic Shock
Some degree of LV dysfunction is expected after an acute MI. The degree of dysfunction correlates with the extent and location of myocardial injury. Patients with small and more distal infarctions may have discrete regional wall motion abnormalities with preserved overall LV function due to hyperkinesis of unaffected segments. Risk factors for development of cardiogenic shock include prior myocardial infarction, older age, female gender, diabetes mellitus, and anterior infarction. [1]
Killip and Kimball[1] developed a classification scheme to predict a patient's prognosis based on their hemodynamic profile. Patients were classified into four hemodynamic subsets; from no evidence of congestive heart failure to cardiogenic shock. They reported an 81% mortality rate in the patients presenting with cardiogenic shock.
Forrester et al. [1] classified patients by their hemodynamic profile with a pulmonary artery catheter. The parameters used included PCWP and cardiac index. They reported a 50% mortality rate in the most compromised subset (PCWP >18 mmHg, cardiac index <2.2 L/min/m2).
According to GUSTO I trial results, 0.8% of patients clinically developed cardiogenic shock. In those receiving fibrinolytics, the mortality rate remained high at 58%.[1]
A complication that may occur in the acute setting soon after a myocardial infarction or in the weeks following it is cardiogenic shock. Cardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a cardiac output to supply an adequate amount of oxygenated blood to the tissues of the body.
While the data on performing interventions on individuals with cardiogenic shock is sparse, trial data suggests a long-term mortality benefit in undergoing revascularization if the individual is less than 75 years old and if the onset of the acute myocardial infarction is less than 36 hours and the onset of cardiogenic shock is less than 18 hours. If the patient with cardiogenic shock is not going to be revascularized, aggressive hemodynamic support is warranted, with insertion of an intra-aortic balloon pump if not contraindicated. If diagnostic coronary angiography does not reveal a culprit blockage that is the cause of the cardiogenic shock, the prognosis is poor.[1]
Pathophysiology of Left Ventricular Failure and Cardiogenic Shock
Patients may develop cardiogenic shock in association with an acute MI from multiple etiologies, including large left ventricular infarction, severe right ventricular myocardial infarction, rupture of ventricular septum, free wall rupture, acute mitral regurgitation, and pharmacologic depression of left ventricular function (e.g. alpha blockers in proximal left anterior descending artery supplied area MI). Patients with cardiogenic shock as a result of acute MI typically have severe multi vessel disease with involvement of the left anterior descending artery.[1]
In general, at least 40% of the left ventricular myocardium is affected in patients who present in cardiogenic shock as a result of a first MI.[1] In patients with prior MIs and depressed LV function, a smaller acute insult may result in cardiogenic shock.
Signs and Symptoms of Left Ventricular Failure and Cardiogenic Shock
Patients who present in Killip-Kimball class 3 often have respiratory distress, diaphoresis, and cool clammy extremities in addition to the typical signs and symptoms of acute MI. Patients in Killip-Kimball class 4 (cardiogenic shock) may have severe orthopnea, dyspnea, oliguria, and altered mental status as well as multisystem organ failure due to hypoperfusion.
It may be possible to palpate the area of dyskinesia on precordium. Additionally, the third heart sound (S3 gallop) is a common physical finding in association with pulmonary rales and elevated jugular venous pressures.
Diagnostic Tests for Left Ventricular Failure and Cardiogenic Shock
Patients with cardiogenic shock due to acute MI generally have extensive ECG changes, demonstrating a large size infarct, diffuse myocardial ischemia, or multiple prior infarcts.
If these changes are not present, then another cause of shock should be considered to clarify the situation. Chest radiograph may reveal acute pulmonary edema, and laboratory tests often demonstrate lactic acidosis, renal failure, and arterial hypoxemia.
The patient in cardiogenic shock should be monitored with a pulmonary artery catheter and an arterial line. These help distinguish between primary left ventricular failure and other mechanical causes of cardiogenic shock. Echocardiography determines the extent of dysfunctional myocardium and helps identify mechanical complications.
Management and Treatment of Patients with Left Ventricular Failure and Cardiogenic Shock
A patient in cardiogenic shock should immediately have an IABP placed to reduce afterload, improve cardiac output, and improve coronary perfusion.
Medical therapy with vasodilators (nitroglycerin, sodium nitroprusside, and angiotensin-converting enzyme inhibitors ACE inhibitors) and diuretics should be used as tolerated.
IV nitroglycerin is the drug of choice among vasodilators for its anti ischemic effects and less likely to produce coronary steal than sodium nitroprusside. The starting dose of nitroglycerin is 10-20 µg/min. The dose then may be increased by 10 µg / min every 2 to 3 minutes to reach a goal of desired mean arterial pressure (MAP) as 70 mmHg.
IV sodium nitroprusside can be added if further reduction in afterload is necessary. Sodium nitroprusside is started at 0.5-1.0 µg/kg/min and is also titrated to an MAP of approximately 70 mm Hg. Patients with low blood pressures (MAP <70 mmHg) may not tolerate vasodilators.
ACE inhibitors improve left ventricular performance and decrease myocardial oxygen consumption by reducing the cardiac preload and afterload of patients with heart failure and acute MI. ACE inhibitors can reduce infarct expansion if started within the first 12 hours of an MI if the patient is not already in cardiogenic shock.[1] [1] It is recommended that captopril be started early at 6.25 mg every 8 hours, with each dose subsequently doubled as tolerated to a maximal dose of 50 mg every 8 hours. Patients in cardiogenic shock should be treated with short-acting IV medications until they are stabilized.
A mild pulmonary edema in patients with MI can be treated with diuretics such as furosemide administered intravenously and adjusted for creatinine and history of diuretic usage. Beta adrenergic receptor agonists (beta stimulant drugs) such as dobutamine or dopamine may be needed for patients with severe heart failure and hypotension. Nevertheless, this therapy should generally be reserved for patients who do not respond to IABP and maximal medical therapy, or those with right ventricular infarction.
Although some patients without adequate mean arterial pressure may not tolerate them, phosphodiesterase inhibitors such as milrinone may be beneficial in those who may tolerate. Some patients may need norepinephrine to maintain arterial pressure. Norepinephrine is started at 2 µg / min and gradually titrated to 20 µg / min to maintain a mean arterial pressure ≥70 mmHg.
Percutaneous coronary revascularization of infarct related artery reducing the mortality rate from 80% to 50% and has been associated with an improved prognosis in patients with cardiogenic shock.
Generally, percutaneous coronary intervention has to be performed only to the IRA, although some report multi vessel percutaneous revascularization with more complete revascularization for patients with refractory shock after IRA recanalization.[1] [1]
Emergency surgical revascularization is indicated in patients with severe multivessel disease or substantial left main coronary artery stenosis. Other surgical modalities that may be considered include LV or biventricular assist devices or extracorporeal membrane oxygenation as a bridge to heart transplantation. Some patients may gradually be weaned from assist devices after recovery of the stunned portion of myocardium without need for cardiac transplantation.
Right Ventricular Failure
Incidence of Right Ventricular Failure
Mild RV dysfunction is common (approximately 40% of cases) after MI of the inferior or inferior-posterior wall; however, right heart failure occurs in only 10% of patients with inferior or inferior-posterior wall MI, normally only in infarcts involving the proximal right coronary artery.
Pathophysiology of Right Ventricular Failure
The degree of right ventricular dysfunction depends on the lesion location of the right coronary artery. Only proximal occlusions (proximal to the acute marginal branch) of the right coronary artery result in marked dysfunction (note: emboli to the acute marginal branch may result in similar results without any visible occlusion). The degree of right ventricular involvement also depends on the amount of collateral flow from the left coronary arteries.
The right ventricle has a thinner wall in comparison to the left one, has a low oxygen demand, and there is continuous coronary perfusion during the entire cardiac cycle, therefore, widespread irreversible infarction is rare in right ventricular myocardium.[1]
Signs and Symptoms of Right Ventricular Failure
The triad of hypotension, jugular venous distention with clear lungs, and absence of dyspnea has high specificity (but low sensitivity) for right ventricular myocardial infarction.[1] Patients with severe right ventricular failure also may present with symptoms of low cardiac output, including diaphoresis, cool and clammy extremities, and altered mental status. Additionally, they often have oliguria and hypotension.
- Physical examination reveals elevated jugular venous pressures, a right sided third heart sound, and normal lung examination on auscultation.
The presence of jugular venous pressure >8 cmH2O and Kussmaul's sign (an exaggerated increase in jugular venous distention with inspiration) is both highly sensitive and specific for severe right ventricular failure. A rare but clinically important complication of the right ventricular myocardial infarction is right-to-left shunting, which is manifested by right ventricular infarction and hypoxemia when right atrial pressures exceed left atrial pressures in patients with a patent foramen ovale.
- Electrocardiographically, patients present with inferior ST elevation in conjunction with ST elevation in V4R (it may be absent in late hours of MI). These findings have 80% positive predictive value for right ventricular myocardial infarction.[1]
- Chest radiographies usually in normal range.
Diagnosis of Right Ventricular Failure
Echocardiography is the diagnostic study of choice for right ventricular infarction. It can detect right ventricular dilatation and dysfunction as well as dysfunction of left ventricular inferior wall. It is also helpful in excluding cardiac tamponade, which may hemodynamically mimic right ventricular infarction. The hemodynamic profile of acute right ventricular infarction is similar to an acute pulmonary embolism.
Hemodynamic monitoring with a pulmonary artery catheter may show high right atrial pressures with a low pulmonary capillaries wedge pressure (unless severe left ventricular dysfunction is present) because right ventricular failure results in under filling of the left ventricle and low cardiac output.
Right ventricular dilatation may cause shifting or bulging of the interventricular septum into the left ventricle, therefore decrease in left ventricular performance (may cause restriction of ventricular filling and elevation of PCWP). A right atrial pressure >10 mmHg and a right atrial pressure to PCWP ratio of 0.8 or more strongly suggest right ventricular infarction.[1] [1]
Management and Treatment of Right Ventricular Myocardial Infarction
Volume loading to increase preload and cardiac output is the key issue in management of right ventricular myocardial infarction. In some patients administration of several liters of fluid may required in an hour to reach the target pulmonary capillary venous pressure (PCWP, 15 mmHg). These patients should have hemodynamic monitoring with a pulmonary artery catheter. The target central venous pressure (CVP) level for fluid administration is approximately 15 mmHg.
When volume loading is insufficient to improve cardiac output and reach this pressure level, positive inotropic agents administrations are indicated. Dobutamine administration increases the cardiac index and improves right ventricular ejection fraction.[1]
Patients who undergo successful reperfusion of right ventricular branches of coronary arteries have enhanced right ventricular function and lower 30 day mortality.[1]
Patients with right ventricular infarction and bradyarrhythmia or loss of sinus rhythm may have significant improvement with AV sequential pacing. Optimal pacemaker settings include longer AV delays (approximately 200 msec) and a heart rate of 80 bpm.
Although only case reports have shown that IABPs improve cardiac index in combination with dobutamine, an IABP may be useful even though it acts primarily on the left ventricle. Pericardiectomy may be considered for patients with refractory shock because it reverses the septal impingement on LV filling. Most patients with right ventricular myocardial infarction spontaneously improve after 48 to 72 hours. An RV assist device is indicated for patients who remain in cardiogenic shock despite these measures.
Ventricular Aneurysm
Incidence of Ventricular Aneurysm in Acute myocardial infarction
Patients with apical transmural myocardial infarctions are at the greatest risk of aneurismal formation; however, patients with posterior-basal infarcts may also develop aneurysms. Patients who do not receive reperfusion therapy are at the greatest risk of developing this complication (10% to 30%).
Pathophysiology of Ventricular Aneurysm in Acute myocardial infarction
The early open artery hypothesis states that early reperfusion results in improved myocardial salvage with inhibition of infarct expansion.
Even late reperfusion limits infarct expansion through multiple mechanisms, including immediate change in infarction characteristics, preservation of residual myofibrils and interstitial collagen, accelerated healing, the scaffold effect of a blood-filled vasculature, and elimination of ischemia in viable but dysfunctional myocardium.
Infarct expansion and progression of left ventricular dilatation are associated with persistent occlusion of the infarct related artery. The aneurysm consists of a stretched portion of the myocardium, containing all three layers and connected with the ventricle by a wide neck.
Signs and Symptoms of Ventricular Aneurysm in Acute myocardial infarction
Congestive heart failure and even cardiogenic shock may develop as a result of a large left ventricular aneurysm. In presence of acute left ventricular aneurysms, the contractile energy generated by normal myocardium is wasted. The aneurysm expands during ventricular systole and causes mechanical disturbances.
If aneurysms persist longer than 6 weeks after the acute event, became less compliant than the acute aneurysms, less likely to expand during systole and named as chronic aneurysm. Patients with chronic aneurysms may have progressive and treatment resistant heart failure, ventricular arrhythmias, and systemic embolism. Sometimes may be even asymptomatic.
Dyskinetic segment of the ventricle may palpable during precordial examination. A third heart sound may be heard in patients with poor ventricular function.
Diagnosis of Ventricular Aneurysm in Acute myocardial infarction
Typical ECG findings include ST segment elevation (no ST segment resolution or occasionally re-elevation), which persists despite reperfusion therapy and Q waves. Prolonged ST segment elevations (persist more than 6 weeks) suggest a chronic formation of ventricular aneurysm.
A chest radiograph may show a ‘’’localized bulge’’’ in the cardiac silhouette.
Echocardiography accurately shows the aneurysmal segment and may also demonstrate the presence of a mural thrombus. Additionally, echocardiography is useful in differentiating true aneurysms from the pseudoaneurysm formation. True aneurysms have a wide neck, whereas pseudoaneurysm has a narrow one in relation to the fundus of the aneurysm.
Cardiac magnetic resonance imaging provides crystal clear images and useful for anatomic description.
Management and Therapy of Ventricular Aneurysm in Acute myocardial infarction
Congestive heart failure with acute aneurysms is managed with IV vasodilators. ACE inhibitors have been shown to reduce infarct expansion and unfavorable left ventricular remodeling.
ACE inhibitors are the most beneficial if they started within 12-24 hours of the onset of acute myocardial infarction to prevent infarct expansion at earlier stages. Administration of corticosteroids and non-steroidal anti-inflammatory agents should be avoided in the acute setting for their demonstrated effects as induction of infarct expansion and aneurysm formation in experimental models.
Heart failure with chronic aneurysms should be managed with ACE inhibitors, digoxin and diuretic therapy.
Anticoagulation with warfarin sodium is indicated for patients with a mural thrombus. Patients should be initially treated with IV heparin with a target partial thromboplastin time of 50 to 70 seconds. Warfarin should be given simultaneously and to maintain the target international normalized ratio of 2-3 for 3 to 6 months.
Anticoagulant treatment of patients with large aneurysms but without any thrombus is controversial. Although, many clinicians prescribe anticoagulants for 6-12 weeks after the acute phase, some of them do not suggest any anticoagulation without a visible thrombus formation.
Patients with left ventricular aneurysms and a low ejection fraction (<40%) have a higher stroke rate and therefore should take anticoagulants for at least 3 months after the acute event. These patients should also have subsequent echocardiographic observations. If thrombus develops, anticoagulation therapy initiated.
Refractory heart failure and ventricular arrhythmias in patients with aneurysms are indication for surgical resection. Surgical resection may be followed by either conventional closure or newer techniques to restore left ventricular geometry.
Coronary revascularization is beneficial for patients with viable myocardium around the aneurysmal segment.
Pathological Findings
Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission. © PEIR, University of Alabama at Birmingham, Department of Pathology
 Left Ventricle Aneurysm: Gross natural color horizontal section apex of left ventricle with aneurysmal dilation and mural thrombus. A large scar tissue in myocardium. |
 Left ventricular aneurysm. |
 Heart; old myocardial infarction with aneurysm formation |
Dynamic Left Ventricular Outflow Tract Obstruction
Incidence of Dynamic Left Ventricular Outflow Tract Obstruction
Dynamic Left Ventricular Outflow Tract Obstruction (LVOT) is an uncommon complication of acute anterior myocardial infarction. [1]
Pathophysiology of Dynamic Left Ventricular Outflow Tract Obstruction
This event is dependent on compensatory hyperkinesias of the basal and mid segments of the left ventricle.
Predictors of enhanced regional wall motion in non-infarct zones are the absence of multi vessel disease, female gender, and higher TIMI flow grades (Thrombolysis in Myocardial Infarction trial) in the infarct related artery. The increased contractile force of these regions decreases the cross-sectional area of the LVOT. The resulting increased velocity of blood through the outflow tract may lower pressure below the mitral valve and result in anterior motion of the leaflet (toward the septum = Venturi effect). This movement may lead to further outflow tract obstruction and mitral regurgitation.
It has been postulated that this complication plays a significant role in free wall rupture. LVOT obstruction leads to increased end systolic intraventricular pressure and therefore increased wall stress of the weak (due to necrosis) infarct zone. This LVOT induced fatal complication occurs most frequently in women, in patients older than 70 years of age, and in those without prior myocardial infarction.
Signs and Symptoms of Dynamic Left Ventricular Outflow Tract Obstruction
Patients may have respiratory distress, diaphoresis, and cool and clammy extremities in addition to the typical signs and symptoms of acute MI. Patients with severe obstruction may appear to be in cardiogenic shock, with severe orthopnea, dyspnea, and oliguria.
They also may have altered mental status from cerebral hypoperfusion. Patients present with a new systolic ejection murmur heard best at the left upper sternal border with radiation to the neck. Additionally, a new holosystolic murmur may present at the apex and radiate to the left axilla as a result of systolic anterior motion of the mitral leaflet. A third heart sound (S3, ventricular gallop), pulmonary rales, hypotension, and/or tachycardia can also be present.
Diagnosis of Dynamic Left Ventricular Outflow Tract Obstruction
Echocardiography is the test of choice. It accurately shows the hyperkinetic segment, the dynamic LVOT obstruction and systolic anterior motion of the mitral leaflet.
Management and Treatment of Dynamic Left Ventricular Outflow Obstruction
Treatment should be focused on decreasing myocardial contractility and heart rate, and expanding intravascular volume to increase the afterload. Beta blockers should be started and titrated gradually with a careful monitoring of heart rate, blood pressure and Svo2. IV hydration with controlled amount of saline solution may be necessary to increase preload and decrease LVOT obstruction and reduce the systolic anterior motion of the mitral leaflet. The patient's hemodynamic and respiratory status should be monitored closely during this therapeutic intervention with a Swan-Ganz catheter. Administration of vasodilators and inotropic agents, and IABP use are not suggested and should be avoided.
C. Arrhythmic Complications of Acute Myocardial Infarction
Dysrhythmia is the most common complication of acute myocardial infarction. It is related to re-entry circuit’s formation. Premature ventricular contractions occur in approximately 90% of patients. The incidence of ventricular fibrillation is approximately 2-4%. Although lidocaine reduces the rate of primary ventricular fibrillation in patients with acute myocardial infarction, there is no survival benefit, and may result in mortality excess. Therefore, lidocaine is not recommended as prophylactic therapy.[1]
Amiodarone may be used in patients with acute myocardial infarction and frequent premature ventricular con